References cited throughout this specification by number are listed at the end of the Examples in the section “REFERENCES”.
Previous studies (1-12) have demonstrated a crucial role for platelet/endothelial cell adhesion molecule-1 [PECAM] in transendothelial migration [TEM] of neutrophils [PMN], monocytes [Mo], and natural killer [NK] cells. However, even under the most favorable circumstances, anti-PECAM reagents block only 80-90% of leukocyte influx. While this is as good or better a block of inflammation as has been achieved by targeting a single molecule, the residual 10-20% of leukocytes that are not blocked may represent a clinically significant population under chronic conditions. Furthermore, there are at least some inflammatory models in which PECAM does not appear to play a role. Most important for the present invention, there may be stages in TEM that are mediated by molecules other than PECAM, which await discovery.